---
title: "Coronary microvascular and myocardial involvement in granulomatosis with polyangiitis: an immunoca"
id: "pubmed-42649433"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42649433"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42649433/"
doi: "10.1007/s00296-026-06282-2"
published_at: "2026-08-27T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Coronary microvascular and myocardial involvement in granulomatosis with polyangiitis: an immunoca
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42649433
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42649433/)
- **DOI:** [10.1007/s00296-026-06282-2](https://doi.org/10.1007%2Fs00296-026-06282-2)
- **Published At:** 2026-08-27T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Granulomatosis with polyangiitis (GPA) is an **ANCA**-associated vasculitis marked by necrotizing inflammation of small- and medium-sized vessels with granulomatous features. - Advances in immunosuppression improved short-term survival but long-term outcomes are limited by cumulative organ damage, treatment toxicity, and excess cardiovascular morbidity and mortality. - Cardiovascular risk in GPA arises from a combination of conventional risk factors, treatment-related metabolic effects, renal dysfunction, systemic inflammation, and disease-associated vascular injury; it likely extends beyond accelerated epicardial atherosclerosis. - Cardiac magnetic resonance (**CMR**) studies in GPA and wider AAV populations report myocardial abnormalities such as **late gadolinium enhancement**, inflammatory changes, and fibrotic remodeling, including in patients without overt cardiac symptoms. - The prevalence, mechanisms, and prognostic significance of **coronary microvascular dysfunction (CMD)** in GPA are not established by current human data. Observations to date are insufficiently specific to confirm CMD as a common or causal process in GPA. - Established AAV pathophysiological components—neutrophil-mediated inflammation, complement activation, endothelial dysfunction, oxidative stress, and thromboinflammatory pathways—are biologically plausible contributors to CMD, impaired myocardial perfusion, and myocardial remodeling in GPA. - Proposed mechanistic links (AAV vascular inflammation → repetitive low-grade ischemia → fibrosis → arrhythmogenesis) are hypothesis-generating and partly extrapolated from experimental models and broader cardiovascular literature. - This review adopts a **GPA-specific**, coronary microcirculation–centered viewpoint, integrating immunopathology and imaging with contemporary CMD and ischemia-with-nonobstructive-coronaries frameworks while distinguishing established findings from proposed mechanisms. - The review highlights potential roles for advanced cardiovascular imaging, individualized risk assessment, and targeted cardiovascular evaluation within an emerging immunocardiology framework. - Prospective GPA-specific studies are needed to define the clinical significance of CMD and to determine whether targeted monitoring or cardioprotective strategies improve outcomes; specific study designs and prevalence estimates were not reported in the source.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Department and Clinic of Cardiology, University of Medical Sciences, 60-545, Poznań, Poland. * 2 Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Sciences, 61-545, Poznań, Poland. * 3 Clinical Rehabilitation Laboratory, Department of Rehabilitation and Physiotherapy, Poznan University of Medical Sciences, 60-545, Poznań, Poland. ewachlebus@ump.edu.pl. * PMID: **42649433** * DOI: [ 10.1007/s00296-026-06282-2 ](https://doi.org/10.1007/s00296-026-06282-2) Item in Clipboard Review # From ANCA-mediated vascular injury to coronary microvascular and myocardial involvement in granulomatosis with polyangiitis: an immunocardiology perspective Mateusz Lucki et al. Rheumatol Int. 2026. Show details Display options Display options Format Abstract PubMed PMID Rheumatol Int Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Rheumatol+Int%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Rheumatol+Int%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) . 2026 Aug 27;46(9):247. doi: 10.1007/s00296-026-06282-2. ### Authors [Mateusz Lucki](https://pubmed.ncbi.nlm.nih.gov/?term=Lucki+M&cauthor_id=42649433)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42649433/#short-view-affiliation-1 "Department and Clinic of Cardiology, University of Medical Sciences, 60-545, Poznań, Poland."), [Bogna Grygiel-Górniak](https://pubmed.ncbi.nlm.nih.gov/?term=Grygiel-G%C3%B3rniak+B&cauthor_id=42649433)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42649433/#short-view-affiliation-2 "Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Sciences, 61-545, Poznań, Poland."), [Ewa Lucka](https://pubmed.ncbi.nlm.nih.gov/?term=Lucka+E&cauthor_id=42649433)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42649433/#short-view-affiliation-3 "Clinical Rehabilitation Laboratory, Department of Rehabilitation and Physiotherapy, Poznan University of Medical Sciences, 60-545, Poznań, Poland. ewachlebus@ump.edu.pl."), [Sylwia Iwańczyk](https://pubmed.ncbi.nlm.nih.gov/?term=Iwa%C5%84czyk+S&cauthor_id=42649433)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42649433/#short-view-affiliation-1 "Department and Clinic of Cardiology, University of Medical Sciences, 60-545, Poznań, Poland."), [Maciej Lesiak](https://pubmed.ncbi.nlm.nih.gov/?term=Lesiak+M&cauthor_id=42649433)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42649433/#short-view-affiliation-1 "Department and Clinic of Cardiology, University of Medical Sciences, 60-545, Poznań, Poland.") ### Affiliations * 1 Department and Clinic of Cardiology, University of Medical Sciences, 60-545, Poznań, Poland. * 2 Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Sciences, 61-545, Poznań, Poland. * 3 Clinical Rehabilitation Laboratory, Department of Rehabilitation and Physiotherapy, Poznan University of Medical Sciences, 60-545, Poznań, Poland. ewachlebus@ump.edu.pl. * PMID: **42649433** * DOI: [ 10.1007/s00296-026-06282-2 ](https://doi.org/10.1007/s00296-026-06282-2) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Granulomatosis with polyangiitis (GPA) is a prototypical antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis characterized by necrotizing inflammation of small- and medium-sized vessels with granulomatous features. Although advances in immunosuppressive therapy have markedly improved short-term survival, long-term outcomes remain limited by cumulative organ damage, treatment-related toxicity, and an excess burden of cardiovascular morbidity and mortality. Cardiovascular risk in GPA appears to reflect a combination of conventional risk factors, treatment-related metabolic effects, renal dysfunction, systemic inflammation, and disease-associated vascular injury and may therefore extend beyond accelerated epicardial atherosclerosis alone. Cardiac magnetic resonance (CMR) studies in GPA and the broader AAV population have identified myocardial abnormalities, including late gadolinium enhancement, inflammatory changes, and fibrotic remodeling, sometimes in patients without overt cardiac symptoms. However, these observations do not establish the prevalence, mechanisms, or prognostic significance of coronary microvascular dysfunction (CMD) specifically in GPA. Neutrophil-mediated inflammation, complement amplification, endothelial dysfunction, oxidative stress, and thromboinflammatory pathways are established components of AAV pathophysiology. Their potential contribution to coronary microvascular dysfunction, impaired myocardial perfusion, and subsequent myocardial remodeling in GPA is biologically plausible but remains insufficiently demonstrated in dedicated human studies. Accordingly, the proposed links between AAV-related vascular inflammation, repetitive low-grade ischemia, fibrosis, and arrhythmogenesis should currently be considered hypothesis-generating and partly extrapolated from experimental AAV models and the broader cardiovascular literature. Unlike previous publications addressing cardiovascular manifestations across the wider AAV spectrum, the present review adopts a GPA-specific and coronary microcirculation-centered perspective. It integrates available immunopathological and imaging evidence with contemporary CMD and ischemia with non-obstructive coronary arteries frameworks while distinguishing established observations from proposed mechanistic relationships. This review also discusses the potential roles of advanced cardiovascular imaging, individualized risk assessment, and targeted cardiovascular evaluation within an emerging immunocardiology framework. Prospective GPA-specific studies are needed to determine the clinical significance of CMD and establish whether targeted cardiovascular monitoring and cardioprotective strategies improve patient outcomes. **Keywords:** Cardiovascular disease; Coronary circulation; Endothelium; Fibrosis; Granulomatosis with polyangiitis; Microcirculation. © 2026. The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Conflict of interest: The authors declare that they have no financial or non-financial interests that could influence the outcomes of this study. There are no competing interests to report. None of the authors has any conflicts of interest to disclose. Consent for publication: The authors consent to the publication of this article. The authors are responsible for the accuracy of the statements contained in the manuscript. Disclaimer: The authors confirm that no part of this manuscript, including the text and graphics, has been copiedor previously published, either in full or in part, elsewhere. This work was prepared solely by the authors withoutthe involvement of any external editing agencies. No AI tools or software were employed in the writing orediting process of this manuscript. Software tools and image creation: The figures were developed by the authors using BioRender, in conjunction with Microsoft Word for illustration editing. The tables were prepared using Microsoft Word, which provided key tools for design and formatting. ## References 1. 1. Jennette JC, Falk RJ, Bacon PA, Basu N, Cid MC, Ferrario F, Flores-Suarez LF, Gross WL, Guillevin L, Hagen EC, Hoffman GS, Jayne DR, Kallenberg CG, Lamprecht P, Langford CA, Luqmani RA, Mahr AD, Matteson EL, Merkel PA, Ozen S, Pusey CD, Rasmussen N, Rees AJ, Scott DG, Specks U, Stone JH, Takahashi K, Watts RA (2013) 2012 revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides. Arthritis Rheum 65(1):1–11. - [DOI](https://doi.org/10.1002/art.37715) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/23045170/) 2. 1. Kallenberg CG (2011) Pathogenesis of ANCA-associated vasculitides. Ann Rheum Dis 70(Suppl 1):i59–63. - [DOI](https://doi.org/10.1136/ard.2010.138024) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/21339221/) 3. 1. Söderberg D, Segelmark M (2016) Neutrophil Extracellular Traps in ANCA-Associated Vasculitis. 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Stone JH, Merkel PA, Spiera R, Seo P, Langford CA, Hoffman GS, Kallenberg CG, St Clair EW, Turkiewicz A, Tchao NK, Webber L, Ding L, Sejismundo LP, Mieras K, Weitzenkamp D, Ikle D, Seyfert-Margolis V, Mueller M, Brunetta P, Allen NB, Fervenza FC, Geetha D, Keogh KA, Kissin EY, Monach PA, Peikert T, Stegeman C, Ytterberg SR, Specks U, RAVE-ITN Research Group (2010) Rituximab versus cyclophosphamide for ANCA-associated vasculitis. N Engl J Med 363(3):221–232. - [DOI](https://doi.org/10.1056/nejmoa0909905) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/20647199/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/3137658/) Show all 66 references ## Publication types * Review Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Review%22%5Bpt%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Review) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) ## MeSH terms * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) * Coronary Circulation Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Coronary+Circulation%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Coronary+Circulation) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) * Coronary Vessels* / immunology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Coronary+Vessels%2Fimmunology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Coronary+Vessels) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) * Coronary Vessels* / physiopathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Coronary+Vessels%2Fphysiopathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Coronary+Vessels) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) * Granulomatosis with Polyangiitis* / complications Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Granulomatosis+with+Polyangiitis%2Fcomplications%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Granulomatosis+with+Polyangiitis) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) * Granulomatosis with Polyangiitis* / immunology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Granulomatosis+with+Polyangiitis%2Fimmunology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Granulomatosis+with+Polyangiitis) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42649433/) * Granulomatosis with Polyangiitis* / physiopathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Granulomatosis+with+Polyangiitis%2Fphysiopathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Granulomatosis+with+Polyangiitis)
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